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The Cardiovascular System > Drugs Used for Cardiac Arrhythmias > Flashcards

Drugs Used for Cardiac Arrhythmias Flashcards

1
Q

How does the SA node initiate depolarisation

A

It can spontaneously depolarise but is under the influence of the sympathetic and parasympathetic nervous system.

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2
Q

What is important in order for the atria to fill the ventricles before they contract

A

The delay introduced by the AV node

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3
Q

What is the role of the perkinje fibres

A

To rapidly transmit the electrical signal through the ventricles

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4
Q

What kind of structure if the myocardium

A

A giant syncytial structure

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5
Q

What part of the bundle of his depolarises the right ventricle

A

The right bundle branch

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6
Q

What part of the bundle of his depolarises the left ventricle

A

The anterior and posterior branches of the left bundle branch of his

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7
Q

What is the state of all of the heart chambers in the quiescent stage of contraction

A

All the myocardium of the ventricles and the atria are repolarised and ready to become depolarised for the next contraction.

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8
Q

What is the P wave on the ECG created by

A

The initial depolarisation from the SA node spreading through the atria

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9
Q

What is the QRS complex on the ECG created by

A

The depolarisation of most of the myocardium

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10
Q

What is the T wave on an ECG created by

A

The repolarisation of the ventricular myocardium

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11
Q

How stable are the cells of the SA node

A

Very unstable - they depolarise spontaneously

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12
Q

How stable are the cells of the myocardium

A

These cells are mostly stable until a depolarising current reaches them.

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13
Q

Which ions influx when there is depolarisation of the cells

A

First sodium ions and then calcium ions.

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14
Q

What ion repolarises the depolarised cells

A

The outflow of potassium ions

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15
Q

How does the heart have one of the highest metabolic demands of any tissue and require the greatest oxygen supply

A

The activities for contraction are very energy intensive.

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16
Q

What are the typical consequences of a cardiac arrhythmia

A

Altered heart rate, usually one which is too fast

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17
Q

What subsequently happens due to fast heart rate

A

Decreased ventricular filling, reduced ejection from the heart and reduced efficiency of the heart - there is less cardiac output for a give amount of work.

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18
Q

What are the clinical consequences of arrhythmias

A
  • A fall in blood pressure
  • A fail in the circulation
  • Anginal pain
  • Heart failure
  • Death
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19
Q

What are the possible appearances on an x-ray as a result of cardiac arrhythmias

A
  • Pulmonary oedema
  • Cardio-thoracic ratio (the width of the heart in relation to the rest of the chest) larger due to dilation of the heart
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20
Q

What are the two general mechanisms of cardiac arrhythmias

A

Increased automaticity and re-entry

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21
Q

How does increased automaticity work to cause cardiac arrhythmias

A

Depolarisation comes from the most unstable cells of the heart. Normally, this is the cells of the SA node. However if one area of myocardium is damaged, for example due to ischaemia, these normally stable cells can become unstable and can depolarise spontaneously. This leads to the heart contracting in a disordered way and results in arrhythmia.

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22
Q

How can re-entry lead to arrhythmia

A

Normally, after the wave of depolarisation travels through part of the heart, this part can no longer respond and depolarise. However, in some instances instead of having to wait for the signal from the SA node, the depolarisation wave can travel round and re-affect part of the heart that would normally be quiescent. This circular motion of activity can go round the heart at a much faster rate than the rate encountered by the depolarisation of the SA node.

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23
Q

What are some clinical causes of arrhythmias

A
  • Coronary artery disease
  • Drugs
  • Electrolyte imbalances
  • Congenital structural abnormalities
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24
Q

How can coronary artery disease lead to arrhythmia

A

Coronary artery disease can lead to ischaemia in the conducting system and myocardium of the heart. This is a problem as oxygen is required to produce ATP and is vital in maintaining stability of cells.

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25
Q

How can drugs lead to arrhythmia

A

Drugs such as beta blockers can cause the heart to run too slow (bradycardia) while other drugs can over-excite the heart result in tachyarrhythmia.

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26
Q

What is the most commonly encountered electrolyte imbalance that leads to arrhythmia

A

An excess or lack of calcium or potassium

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27
Q

What are two examples of atrial arrhythmias

A

Atrial fibrillation, atrial flutter

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28
Q

What is an example of an arrhythmia of the AV node

A

Supraventricular tachycardia

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29
Q

What are two examples of ventricular arrhythmias

A

Ventricular tachycardia and ventricular fibrillation

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30
Q

What are the three types of heart block

A

First degree heart block, second degree heart block and complete heart block.

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31
Q

What will a patient with atrial fibrillation complain of

A

Breathlessness and palpitations

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32
Q

What is the typical presentation of someone with atrial fibrillation

A

heart failure and pulmonary oedema and possible angina chest pain.

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33
Q

What is the fastest rate at which the AV node can conduct impulses

A

200 per minute

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34
Q

What are the clinical examinations that should be carried out for suspected atrial fibrillation

A

Find the radial pulse. This will be irregularly irregular. Also, if you listen to the heart at the same time and listen for the closing of the aortic valve, there may not be a pulse at the radial artery on every occasion.

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35
Q

What are the causes of atrial fibrillation

A
  • Ischaemic heart disease
  • Hyperthyroidism
  • Rheumatic fever
  • Cardiomyopathies
  • Pulmonary embolism
  • Atrial-septal defects
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36
Q

In what group is atrial fibrillation most common

A

The elderly

37
Q

What drugs can be used to treat atrial fibrillation

A

Digoxin, beta-blockers and calcium channel blockers

38
Q

What kind of drugs are used for people with atrial fibrillation due to the higher risk of thromboembolism

A

Anti-coagulant drugs such as warfarin

39
Q

What surgical procedures can be used for treatment of atrial fibrillation

A

Cardioversion and catheter ablation

40
Q

How does digoxin work

A

It inhibits the sodium potassium pump on cell membranes. This increases sodium within the cell which inhibits co-transport of sodium and calcium. This increases the availability of calcium for use by the contractile apparatus in the ventricular myocardium so ventricular pumping becomes more forceful

41
Q

What are the therapeutic actions of digoxin

A

Decrease conduction through the AV node and increase the force of contraction for improved efficacy of contraction.

42
Q

What is digoxin used for

A

Atrial fibrillation, sinus rhythm, heart failure

43
Q

How is digoxin given

A

Orally or IV

44
Q

What does the fact that digoxin has a long half life mean for drug doses

A

A loading dose may need to be used if rapid action is required

45
Q

What are the adverse effects of digoxin

A
  • Upset of the GI system
  • Visual disturbances - yellow discolouration
  • can be pro-arrhythmic as opposed to anti-arrhythmic - may cause AV block or tachycardia
46
Q

What kind of drugs does digoxin have an adverse reaction with and what is the mechanism of this

A

Diuretics can waste potassium from the body leading to hypokalaemia. Toxicity of digoxin is promoted if the patient has hypokalaemia so there is an adverse effect of using digoxin alongside diuretics.

47
Q

What condition means that digoxin needs to be used with caution

A

Renal failure because it depends largely on renal excretion to be removed from the body.

48
Q

Where do beta-blockers act

A

Beta-1 receptors on the heart

49
Q

What do beta-1 adrenoceptors on the heart normally respond to

A

Adrenaline and other catecholamines as part of the sympathetic and parasympathetic nervous system.

50
Q

What are three examples of non-selective beta-blockers

A

Atenolol, bisoprolol and metoprolol

51
Q

What is an example of a non-selective beta-blocker

A

Propanolol

52
Q

What is the mechanism of action of beta-blockers

A

To reduce the sympathetic nervous system activity and its effect on the conduction system of the heart to reduce excitability and ventricular response rate.

53
Q

What conditions are beta-blockers used for

A

Atrial fibrillation, hypertension and angina.

54
Q

What are the adverse effects of beta-blockers

A
  • Lethargy
  • Bronchospasm
  • Decreased peripheral perfusion
  • Hypotension
  • Heart block
55
Q

What are the presentations of supraventricular tachycardia

A

Rapid palpitations, often in younger people

56
Q

What is the mechanism of supraventricular tachycardia

A

Rapid re-entry through the AV node. There is an anatomical defect called a bypass tract through which conduction can occur from the atria to the ventricles.

57
Q

In what situation does the presence of a bypass tract lead to pathology

A

If the bypass tract is no longer refractory and send depolarisation back through the atrial myocytes and through the AV node again. The ventricles respond to the bypass circuit as opposed to the SA node conduction.

58
Q

What non-pharmalogical method can be used in the treatment of supraventricular tachycardia

A

Stimulate the parasympathetic nervous system at the vagus nerve. ACh can be released and slow down the conduction system.

59
Q

How can you stimulate the parasympathetic nervous system in order to treat supraventricular tachycardia

A

A carotid sinus massage, valsalve manoeuvre, pressure over the eyeballs and the diving reflex.

60
Q

What pharmalogical methods can be used in the acute treatment of supraventricular tachycardia

A

Adenosine or verapamil

61
Q

How does adenosine work in the acute treatment of supraventricular tachycardia

A

It decreases conduction through the AV node. It is rapidly cleared by the body so the effect only lasts a few seconds but this may be enough to allow the SA node to take over the rhythm again.

62
Q

When is cardioversion used

A

Cardioversion is used in supraventricular tachycardia when the patient is compromised, for example if they have low blood pressure or are semi-conscious.

63
Q

What is cardioversion

A

A surgical procedure in which everything is depolarised allowing recovery time and conduction to begin from the start again.

64
Q

What are the long term treatments for supraventricular tachycardia

A

Regular oral verapamil

65
Q

What is the mechanism of action of adenosine

A

It acts on adenosine receptors particularly in the AV node where is facilitates the activity of the potassium channels. This prevents conduction for a short period of time and temporarily abolishes re-entry through the AV node.

66
Q

How can adenosine be used for diagnosis of supraventricular tachycardia

A

If you are unsure whether the arrhythmia is supraventricular tachycardia or ventricular arrhythmia, use adenosine and if nothing happens, it is very unlikely to be supraventricular tachycardia.

67
Q

What are the adverse effects of adenosine

A

Chest pain and breathlessness, however these effects are short lived.

68
Q

What is verapamil

A

A centrally acting calcium channel blocker.

69
Q

What does verapamil do

A

It works on voltage gated calcium channels and decreases the conduction in the SA and AV nodes and also reduces the force of contraction of the heart. It also causes some degree of peripheral vasodilation.

70
Q

What is verapamil used for

A

Supraventricular tachycardia, angina and hypertension.

71
Q

What are the adverse effects of verapamil

A

Constipation due to relaxation of GI smooth muscle, heart block, bradycardia, reduced blood pressure.

72
Q

What class of drugs do calcium channels have a very serious interaction with

A

Beta-blockers

73
Q

Why is there a serious interaction between beta-blockers and calcium channel blockers

A

Because both of these drugs inhibit the conduction system and there is a risk of completely blocking the conduction through the AV node leading to cardiac arrest.

74
Q

What is ventricular tachycardia

A

A series of three or more ventricular ectopic beats. The beats are driven within the ventricles as opposed to the normal mechanism.

75
Q

What can sustained ventricular tachycardia lead to

A

Hypotension, heart failure, ventricular fibrillation and cardiac arrest.

76
Q

What is the cause of ventricular tachycardia

A

Myocardial ischaemia

77
Q

What is one of the most common causes of ventricular arrhythmias

A

A failing dilated heart.

78
Q

What can be signs of an MI on an ECG trace

A

ST elevation or the development of Q waves.

79
Q

What is used in the acute treatment of ventricular tachycardia

A

Lidocaine, amiodarone, procainamide,

80
Q

What is performed on the heart if the patient is compromised to restore normal sinus rhythm

A

Cardioversion

81
Q

What is the name of a drug mainly used as a local anaesthetic but which can also be used as an anti-arrhythmic

A

Lidocaine

82
Q

What does lidocaine do

A

Blocks sodium channels in excitable tissues.

83
Q

By what method should lidocaine not be taken and why

A

Orally because it is 0% bioavailable when taken this way.

84
Q

What are the adverse effects of lidocaine

A

Depression of the excitable tissue - on the heart and the central nervous system. This can cause confusion, drowsiness and convulsions.

85
Q

What is the mode of action of amiodarone

A

It prolongs an action potential by blocking potassium channels which repolarise the cells.

86
Q

What does amiodarone contain

A

Iodine

87
Q

Why is amiodarone a very effective anti-arrhythmic

A

It works on the atria and the ventricles so is used for atrial fibrillation as well as ventricular arrhythmias

88
Q

What is the negative about giving amiodarone

A

It is extensively bound to tissues so takes a long period of time to load up and to leave the system. A loading dose can be given if required. It is also very toxic

89
Q

What are the adverse effects of amiodarone

A
  • micro-deposits in the cornea
  • photosensitivity
  • slate-grey discolouration of the skin
  • pneumonitis
  • pulmonary fibrosis
  • peripheral neuropathy
  • thyroid dysfunction
  • hepatitis

The Cardiovascular System (15 decks)

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